Acute Bacterial Myocarditis Masquerading ST Elevation Myocardial Infarction (STEMI): Case Report
Mohamud Mire Waberi*, Abdu Samad Mohamed Aden, Abdiwali Awil Dahir, Mohamed Abdirahman Farah and Mohamed Omer Hassan
Acute Bacterial Myocarditis Masquerading ST Elevation Myocardial Infarction (STEMI): Case Report
Mohamud Mire Waberi1*, Abdu Samad Mohamed Aden2, Abdiwali Awil Dahir3, Mohamed Abdirahman Farah4 and Mohamed Omer Hassan1
1Department of Cardiology, Mogadishu Somali Turkish Training and Research Hospital, Somalia
2Department of internal Medicine, Mogadishu Somali Turkish Training and Research Hospital, Somalia
3Department of Emergency Medicine, Mogadishu Somali Turkish Training and Research Hospital, Somalia
4Department of Neurosurgery, Mogadishu Somali Turkish Training and Research Hospital, Somalia
*Corresponding author
Mohamed Mire Waberi, Department of Cardiology, Mogadishu Somali Turkish Training and Research Hospital, Somalia.
ABSTRACT
Infections are among the many coexisting medical conditions that might result in acute myocarditis. Viral infections cause most of these cases, however bacterial infections do play a role occasionally. Group A streptococcus is often responsible for bacterial myocarditis. This case report discusses the case of a 34-year-old male who had acute streptococcal myocarditis and tonsillitis. An acute myocardial infarction was initially diagnosed based on clinical, enzymatic, and electrocardiographic data.
Introduction
An inflammation of the heart myocytes known as myocarditis can cause range from minor symptoms to life-threatening conditions like dilated cardiomyopathy. It is a different form of myocardial infraction that is due to reduced blood flow caused by the narrowed lumen [1,2].
Most cases in previously healthy individuals are caused by infectious disease, which can be caused by a direct viral infection or by a post-viral immune-mediated reaction [3].
Group A streptococcus (GAS) is rarely reported as the etiological agent of acute myocarditis in the absence of signs and symptoms indicating rheumatic fever. At this point, there are no epidemiological statistics estimating the incidence of myocarditis caused by GAS. Myocardial inflammation and damage are believed to be mostly caused by IgG-binding proteins produced by GAS antigens that cross-react with cardiac myosin [4]. Based on the clinical course, it can be divided into two main categories: fulminant and non-fulminant variants. The prognosis is worse for the fulminant kind, which manifests as severe heart failure requiring inotropic or mechanical circulatory support [5].
However, the vast majority of people demonstrate no symptoms. Of those with symptoms, 72% have dyspnea, 32% experience chest tightness, and 18% experience arrhythmias or even sudden cardiac death [6].
We report the case of a 34-year-old man who was admitted to the hospital due to acute ST-elevation myocardial infarction and typical cardiac chest discomfort. Subsequent testing revealed that acute nonrheumatic streptococcal myocarditis was the cause of his main complain.
Case Presentation
A 34-year-old man presented to the hospital complaining a 3-day history of sore throat, cough, and back pain radiating to the chest. The patient had no significant risk factors for cardiovascular disease.
On admission, his electrocardiogram showed a sinus rhythm with a rate of 100 beats per minute and ST elevations in leads II, AVF, V3- V6 (Figure 1). Troponin I level was found to be elevated at 0.5 ng/mL. A repeat troponin I level was markedly increased at 3.5 ng/mL. Transthoracic echocardiogram demonstrated preserved left ventricular systolic function with an ejection fraction of 60% and no regional wall motion abnormalities. There were no apparent chamber dilatations or valvular regurgitations. Percutaneous coronary angiography revealed no evidence of obstructive coronary artery disease (Figure 2). Cardiac MRI with gadolinium showed normal Left Ventricular size with 55% Ejection fraction, patchy mid-myocardial and epicardial delayed gadolinium enhancement with superimposed edema (Figures 3 a and b), the patient was assumed to have non-rheumatic streptococcal myocarditis. While awaiting the results of the swab culture, an empirical antibiotic therapy was initiated; the culture revealed a group A streptococcal infection. After two days, the patient was discharged with Augmentin 1000mg twice daily for two weeks. After five months of follow up he was well.
Discussion
Myocarditis is an inflammation of the heart accompanied by surrounding myocyte necrosis and degeneration [7]. The incidence of myocarditis is estimated to be between 10 to 20 cases per 100,000 persons [8].
Additionally, it has been noted that myocarditis frequently manifests in younger patients without the usual risk factors for accelerated atherosclerosis opposite to acute coronary syndrome which has both modifiable and non-modifiable risk factors [9,10].
Myocarditis was discovered to be the most common cause of acute coronary syndrome with normal coronary arteries in young and middle-aged patients [11].
Myocarditis is most usually caused by viral infection, with adenovirus and enterovirus being the most frequently found viruses. Apart from autoimmune diseases including lupus, sarcoidosis, lymphocytic myocarditis, and giant cell myocarditis, other etiologies can be caused by bacteria, protozoa, poisons, medication responses, and cancer [12].
Acute rheumatic fever is the term most frequently used to explain the link between streptococcal infection and cardiac disease; nevertheless, some published case reports indicate concurrent streptococcal pharyngitis and myocarditis, also known as acute non-rheumatic streptococcal myocarditis. In the biggest case series, 35 occurrences of fatal myocarditis in men between the ages of 20 and 30 were linked to nasopharyngeal infections. streptococcal pharyngitis and/or streptococcal bacteremia was demonstrated in 12 of these patients. Since that publication, there have been at least 30 other cases described in the literature, predominately in young men [13].
Acute myocarditis remains one of the most challenging diagnoses in cardiology. In patients with suspected myocarditis, magnetic resonance imaging (MRI) has become popular as the diagnostic tool of preference for detecting acute myocardial injury and necrosis [14].
The Consensus Criteria for Cardiovascular Magnetic Resonance (CMR) in Myocardial Inflammation ("Lake Louise Criteria") was published in 2009(2). These criteria suggested three diagnostic targets in myocardial tissue based on signal intensity assessment in T2-weighted, early gadolinium enhancement (EGE), and late gadolinium enhancement (LGE) CMR images: edema, hyperemia, and necrosis or scar. A high likelihood of acute myocarditis is indicated if the CMR images are positive for 2 out of 3 criteria [15].
Invasive endomyocardial biopsy is only suggested in patients with evidence of heart failure in combination with acute disease (2 weeks, class I) or left ventricular dilatation (3 months, class I) or specific other cases of heart failure. (Class IIa) [16].
Although a negative biopsy does not rule out active viral myocarditis, it is useful in establishing the diagnosis and directing treatment in patients with fulminant new-onset heart failure, for example, when giant cell myocarditis is suspected [17].
Conclusion
This example illustrates the difficulty in diagnosing acute myocarditis, as myocarditis is not always a straightforward diagnosis. Sometimes, it manifests as localized ST-segment elevation ECG abnormalities that mimic a myocardial infarction and chest discomfort. Myocarditis should be considered a serious differential diagnosis if a young patient with no significant cardiovascular risk factors shows up to the emergency room complaining of chest discomfort and an ST-segment elevation on the ECG. For the purpose of diagnosing and treating myocarditis in a timely manner, a complete history, physical examination, and relevant investigations are essential.
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